We propose that cardiac ischemia resulting from coronary artery occlusion produces alteration in sympathetic activity to the heart as well as prostaglandin release. The prostaglandins released could have variable and possibly biphasic effects on the sympathetic nerves in the heart. We further propose that the prostaglandins released from ischemic areas of the heart differ and that their effect on cardiac rhythmicity differ depending on the type of interaction with cardiac sympathetic nerves. If the interaction between prostaglandin, cardiac sympathetic nervous activity and cardiac rhythm after coronary occlusion can be elucidated, it may be possible to develop therapeutic agents to manipulate this system and alter the arrhythmia sequelae of acute coronary artery occlusion.